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PubMed1993

Models of cognitive mediation and moderation in child depression.

Negative cognitive errors, attributional style, positive and negative events, peer-nominated competence, and self-reported depression were assessed in 356 fourth, sixth, and eighth graders. Data supported theoretical models in which attributional style and cognitive errors mediated the relation of competence to depression. Data did not support models in which attributional style moderated the relation between either life events or competence and depression; however, weak support emerged for a moderational model involving negative life events and cognitive errors. The viability of diathesis-stress models in childhood, especially in which cognitive style is the diathesis, is critically examined.

Adolescent↗
PubMed1985

Passive avoidance in syndromes of disinhibition: psychopathy and extraversion.

According to the physiological animal model proposed by Gorenstein and Newman (1980; see also Newman, Gorenstein, & Kelsey, 1983), psychopaths and extraverts may be characterized by a common psychological diathesis related to behavioral inhibition (see also Fowles, 1980; Gray, 1982). One aspect of this diathesis involves deficient passive avoidance learning, which has been central to explanations of "unsocialized" (e.g., Trasler, 1978) and antisocial behavior (e.g., Hare, 1970). Results from three experiments supported our prediction that psychopaths and extraverts would exhibit deficient passive avoidance relative to nonpsychopaths and introverts, respectively. In addition, the passive avoidance deficit was particularly evident in tasks that required subjects to inhibit a rewarded response in order to avoid punishment. The latter finding may be important for explaining the inconsistent results regarding passive avoidance learning in psychopaths (e.g., Chesno & Kilmann, 1975; Schmauk, 1970). Discussion of the results focuses on the importance of reward in mediating the passive avoidance deficit of "disinhibited" individuals and on the existence of an indirect relationship between psychopathy and extraversion: one that is consistent with the observed experimental parallels as well as with the more ambiguous evidence regarding a direct correlation between measures of the two syndromes.

Adolescent↗
PubMed2006

Frontal EEG asymmetry and premenstrual dysphoric symptomatology.

Resting frontal electroencephalographic (EEG) asymmetry has been hypothesized to tap a diathesis toward depression or other emotion-related psychopathology. Frontal EEG asymmetry was assessed in college women who reported high (n = 12) or low (n = 11) levels of premenstrual negative affect. Participants were assessed during both the follicular and the late luteal phases of the menstrual cycle. Women reporting low premenstrual dysphoric symptomatology exhibited greater relative left frontal activity at rest than did women high in premenstrual dysphoric symptomatology, an effect that was not qualified by phase of cycle. Although women with extreme levels of symptomatology were assessed, the question of whether such symptoms qualified for premenstrual dysphoric disorder criteria was not assessed. These results are consistent with a diathesis-stress model for premenstrual dysphoric symptomatology.

Adult↗
PubMed2002

Impact of calcium antagonists on bleeding time in patients with chronic renal failure.

Haemorrhagic diathesis develops in chronic renal failure, in which calcium antagonists are used widely as antihypertensive agents. Although calcium antagonists are reported to impair platelet function, it has not been examined whether calcium antagonists alter bleeding time. The present study was conducted to clarify whether calcium antagonists affect bleeding time in chronic renal failure. Patients with chronic renal failure without and with calcium antagonists were enrolled (n = 156), and bleeding time (Ivy's method) as well as blood parameters (BUN, creatinine, platelet counts, and haemoglobin) were compared in patients with normal and prolonged bleeding time. Among patients not taking calcium antagonists (n = 34), three cases manifested prolonged bleeding time, whereas abnormal bleeding time was observed in 31 patients out of 122. Positive correlations were observed between bleeding time and BUN in both calcium antagonist-untreated (r = 0.46) and -treated groups (r = 0.25). The odds ratio for prolongation of bleeding time in patients taking calcium antagonists was 3.52 (95% CI, 1.01-12.33). In 12 calcium antagonist-treated patients with prolonged bleeding time, the withdrawal of calcium antagonists markedly shortened bleeding time (from 11.3 +/- 0.8 to 5.4 +/- 0.8 min, P < 0.05, n = 12). In contrast, in the additional group (n = 9), the continued treatment with calcium antagonists had no effect on bleeding time (from 11.7 +/- 0.9 to 10.0 +/- 1.0 min). Despite the inhibitory effect of calcium antagonists on bleeding time, no clinically serious events associated with haemorrhagic diathesis developed. In conclusion, calcium antagonists prolong bleeding time in patients with chronic renal failure. The subclinical (laboratory) effect of calcium antagonists however is not necessarily associated with haemorrhagic events of clinical significance.

Aged↗
PubMed1998

Protein Z in healthy human individuals and in patients with a bleeding tendency.

Protein Z is a vitamin-K-dependent plasma glycoprotein; its physiological function is not clear. Low protein Z levels were found in patients with otherwise unexplained bleeding disorders. It was therefore suggested that low protein Z levels might be associated with a bleeding diathesis. In the present study we measured protein Z levels in plasma samples of 48 patients with a suspected bleeding disorder and in plasma samples of 200 healthy adult individuals. We found protein Z to have a wide normal range in healthy men and women. Significantly lower protein Z levels were observed in women compared to men, whereas no correlation was found with age or other vitamin-K-dependent coagulation proteins. None of the 48 patients with a bleeding disorder had a protein Z level below the normal range. However, protein Z was significantly lower in the group of male patients with a bleeding history as compared to healthy men. In conclusion, our data indicate that low-normal protein Z levels are not associated with a bleeding tendency. However, it remains to be determined whether a low protein Z level is a weak cofactor associated with an increased bleeding tendency and whether decreased or absent protein Z (conditions not detected in our patients) might constitute a haemorrhagic diathesis.

Adolescent↗
PubMed1998

A new variant of Bernard-Soulier syndrome characterized by dysfunctional glycoprotein (GP) Ib and severely reduced amounts of GPIX and GPV.

We describe a new variant of Bernard-Soulier syndrome characterized by almost normal amounts of GPIb and severely reduced GPIX and GPV. Despite surface expression, GPIbalpha failed to support ristocetin-induced platelet agglutination and to bind two conformation-dependent monoclonal antibodies, suggesting a qualitative defect. Sequence analysis of the gene coding for GPIX revealed a T-to-C substitution at base 1811, leading to a Leu40Pro conversion, whereas no defects were found in the coding region of the GPIbalpha gene. Allele-specific restriction enzyme analysis showed that the propositus and one of his sisters. both with severe bleeding diathesis. were homozygous for the GPIX mutation: the members of the family with mild bleeding diathesis and/or giant platelets in the peripheral blood were heterozygous, whereas the healthy ones were homozygous for the normal allele. Infusion of 1-desamino-8-D-arginine vasopressin normalized bleeding time in the two severely affected patients, although it did not modify ristocetin-induced platelet agglutination or membrane expression of GPIbalpha, GPIX, GPIIb-IIIa and GMP-140. Moreover, in one patient, normalization of bleeding time and rise of von Willebrand factor plasma concentration did not seem to be directly related.

Amino Acid Substitution↗
PubMed2003

Lupus anticoagulant associated with transient severe factor X deficiency: a report of two patients presenting with major bleeding complications.

Acquired factor X (FX) deficiency is rare, but has been reported in diverse disease states, including systemic amyloidosis and respiratory infections. FX deficiency associated with lupus anticoagulant (LA) and a bleeding diathesis has not been previously reported. We report two patients both of whom presented with a severe bleeding diathesis after a preceding respiratory infection due to isolated FX deficiency associated with a LA. The FX deficiency and LA were transient. We conclude that patients with LA may rarely present with severe acquired FX deficiency. This may be another mechanism whereby patients with antiphospholipid antibodies present with bleeding complications.

Antibodies, Antiphospholipid↗
PubMed2001

Depressogenic cognitive schemas: enduring beliefs or mood state artefacts?

OBJECTIVE: The objective of this study was to review findings from a previously posited 'lock and key' hypothesis which challenge a number of assumptions about cognitive theories of depression. METHOD: A review of existing cognitive vulnerability theories is presented. Two recent studies employed to test the lock and key hypothesis are summarized. The hypothesis is reviewed in light of other diathesis-stress models of cognitive vulnerability. RESULTS: The identification of a depressed individual's core beliefs or cognitive schemas is a difficult task, with perhaps unresolvable difficulties in disentangling any mood state determinant. Longitudinal assessment of originally euthymic subjects appears the best method to investigate any cognitive risk to depression and the significance of diathesis-stress models. CONCLUSIONS: Empirical evidence for or against the validity of cognitive vulnerability theories is largely dependent upon the methodologies used to detect cognitive styles, as well as the nature of the subject groups studied.

Affect↗
PubMedDate not supplied

The association of a HOPA polymorphism with major depression and phobia.

Thyroid hormone has a prominent role in the development and homeostasis of the central nervous system (CNS). Consequently, genes participating in thyroid hormone receptor (THR)-mediated signal transduction are prime candidates for neuropsychiatric illness susceptibility factors. Previously, we have associated exonic polymorphisms in a Xq13 thyroid receptor coactivator named HOPA with a modest increase in vulnerability to a broad spectrum of neuropsychiatric illness, including depression, psychosis, and hypothyroidism. In order to test and extend these findings, we have now examined the relationship between HOPA polymorphisms and neuropsychiatric illness in a cohort of Iowa adoptees. Consistent with our prior findings, HOPA polymorphisms were associated with an increased risk for major depression. There was suggestive evidence that the increased psychiatric morbidity in these subjects could represent epistasis, e.g., an interaction between the HOPA variant and a genetic diathesis for another psychiatric condition such as biologic parent antisocial behavior. Information about biologic parent behavior and the adoptive home environment was used to determine depressive symptoms attributable to gene-environment interaction. HOPA variant subjects continued to show significant differences in depressive symptoms when controlling for gene-environment interaction. Finally, because obesity is associated with hypothyroidism and HOPA polymorphisms are associated with hypothyroidism, we analyzed weight with respect to HOPA allele status. We found that that HOPA polymorphisms were associated with increased risk for obesity (P <.001). In summary, we conclude that HOPA polymorphisms may be a moderate risk factor for increased susceptibility to a broad spectrum of neuropsychiatric illness and hypothesize that the type of illness manifested might be related to a separate genetic diathesis.

Adoption↗
PubMed1999

[Neurobiological correlates of suicidal behavior].

Studies in postmortem brain tissue from suicide victims show a presynaptic serotonergic deficit resulting in compensatory upregulation of postsynaptic 5-HT2 receptors in the prefrontal cortex. Reduced levels of cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid, the major serotonin metabolite, are associated with violent suicide attempts independent of psychiatric diagnosis and predict future suicide attempts and suicide completion, consistent with the notion of a biochemical trait. Neuroendocrine challenge tests, platelet studies and a polymorphism in the gene for tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, suggest that serotonergic activity may be reduced. This serotonergic abnormality might be related to the vulnerability or diathesis for suicidal behaviour by predisposing individuals to impulsive and autoaggressive behaviour. The hypothesis of hyperactivity of the hypothalamic pituitary adrenal axis (HPA) is supported by the postmortem findings of increased CSF corticotropin releasing hormone (CRH) concentrations and reduced CRH receptor binding sites in the frontal cortex of suicide victims (interpreted as downregulation following CRH hypersecretion) and dexamethasone nonsuppression in suicide attempters. Animal studies and in vitro experiments indicate that the HPA system modulates serotonergic activity. It is hypothesized that the serotonergic alterations potentially result from dysregulation of the HPA system. Data from epidemiological and clinical studies demonstrate that low levels of cholesterol are associated with increased suicide risk. In neuronal membranes cholesterol modulates presynaptic and postsynaptic serotonergic neurotransmission. In monkeys dietary cholesterol lowering inhibits central serotonergic activity and predisposes the animals to impulsive and aggressive behaviour. It is speculated that dysregulation of the HPA system and disordered cholesterol metabolism could enhance the serotonergic deficit, thus contributing to a neurobiological vulnerability or diathesis for impulsive and autoaggressive behaviour.

Animals↗
PubMed2000

Hematopoietic reconstitution of SLP-76 corrects hemostasis and platelet signaling through alpha IIb beta 3 and collagen receptors.

Mice deficient in the hematopoietic cell-specific adapter protein SLP-76 demonstrate a failure of T cell development and fetal hemorrhage. Although SLP-76-deficient platelets manifest defective collagen receptor signaling, this alone may not explain the observed bleeding diathesis. Because alpha IIb beta 3, the platelet fibrinogen receptor, is required for normal hemostasis, we explored a potential role for SLP-76 in alpha IIb beta 3 signaling. Interaction of soluble or immobilized fibrinogen with normal human or murine platelets triggers rapid tyrosine phosphorylation of SLP-76. Moreover, platelet adhesion to fibrinogen stimulates actin rearrangements, filopodial and lamellipodial extension, and localization of tyrosine phosphorylated proteins to the cell periphery. In contrast, SLP-76-deficient murine platelets bind fibrinogen normally, but spread poorly and exhibit reduced levels of phosphotyrosine. The in vivo bleeding diathesis as well as the defects in platelet responses to fibrinogen and collagen are reversed by retroviral transduction of SLP-76 into bone marrow derived from SLP-76-deficient mice. These studies establish that SLP-76 functions downstream of alpha IIb beta 3 and collagen receptors in platelets. Furthermore, expression of SLP-76 in hematopoietic cells, including platelets, plays a necessary role in hemostasis.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Hermansky-Pudlak syndrome with colitis and pulmonary fibrosis.

Hermansky-Pudlak syndrome (HPS) is a rare autosomal recessively inherited disease with oculocutaneous albinism, hemorrhagic diathesis, and multisystemic deposition of ceroid lipofuscin. We report a case with all symptoms characteristic of HPS. The patient was a mentally retarded albino with mild bleeding diathesis, and her course was complicated by granulomatous colitis refractory to medical treatment and progressive, fatal pulmonary fibrosis.

Adult↗
PubMed2000

Haemophilia A in a litter of Siberian huskies.

AIM: To investigate haemorrhagic diathesis in several males in a litter of Siberian huskies. METHODS: Activated partial thromboplastin time, prothrombin time, and Factor VIII and Factor IX concentrations were measured in citrated whole blood samples. RESULTS: Males in the litter had decreased Factor VIII concentrations. CONCLUSIONS: Haemophilia A was diagnosed as the cause of haemorrhagic diathesis in several males in a litter of Siberian huskies.

Journal Article↗
PubMed1989

Antioxidant activity of dietary canthaxanthin.

It has been suggested that canthaxanthin (CX), beta-carotene, and other carotenoids may inhibit carcinogenesis via antioxidant activity. CX has been shown to inhibit lipid peroxidation in liposomes; this experiment was designed to assess the antioxidant activity of CX in biological membranes. Chicks were fed semipurified diets supplemented with placebo beadlets or CX beadlets (5 g beadlets/kg diet; 0.5 g CX/kg diet) for five weeks. Diets were deficient in vitamin E and selenium to maximize the power of detecting an antioxidant effect of CX and to induce exudative diathesis, which is a vitamin E and selenium deficiency disease of chicks. Dietary CX had no effect on the onset, incidence, or severity of exudative diathesis. Liver homogenates from CX-fed chicks exhibited significantly (p = 0.02) decreased formation of thiobarbituric acid-reactive substances over time in ferrous ion-induced peroxidations. Because dietary CX increased hepatic alpha-tocopherol content, subsequent peroxidations were conducted in membrane fractions prepared from placebo and CX livers matched for alpha-tocopherol content. In this system, CX was marginally but inconsistently protective against peroxidation at both 15 torr O2 (p = 0.12) and 150 torr O2 (p = 0.07). Nanomolar changes in hepatic alpha-tocopherol, unlike CX, substantially altered rates of peroxidation. These results suggest that under these conditions, dietary CX increased resistance to lipid peroxidation primarily by enhancing membrane alpha-tocopherol levels and secondarily by providing weak direct antioxidant activity.

Animals↗
PubMed2005

Social context in gene-environment interactions: retrospect and prospect.

While many behavioral scientists believe that gene-environment (GE) interactions play an important and perhaps pervasive role in human development and aging, little attention has been devoted to a fundamental conceptual issue: What is it about social context that could alter gene expression? We draw on existing examples of GE interactions to formulate a typology that identifies a set of generic mechanisms by which E moderates G. Empirical studies suggest four ideal types: Social context can trigger a genetic diathesis, compensate for a genetic diathesis, act as a control to prevent behaviors for which there is a genetic predisposition, and enhance adaptation through proximal processes. This typology highlights several problems, however, with prior empirical research, which may explain, in part, why so few GE interactions have actually been observed. These problems include inattention to the dynamic nature of social experience, the manifold, often-intercorrelated dimensions of social context ("EE interactions"), mediators that link social context and the genotype, and analytic models that examine GE interactions as processes that characterize individual development. In turn, these insights call for the integration of life course sociology and behavioral genetics to foster ways of studying genes, context, and aging.

Aging↗
PubMed2003

The stress cascade and schizophrenia: etiology and onset.

Psychosocial stress is included in most etiologic models of schizophrenia, frequently as a precipitating factor for psychosis in vulnerable individuals. Nonetheless, the stress-diathesis model has not been tested prospectively in prodromal patients as a predictor of psychosis. The biological effects of stress are mediated by the hypothalamic-pituitary-adrenal (HPA) axis, which governs the release of steroids, including cortisol. The past few decades have witnessed an increased understanding of the neural effects of stress and cortisol, including both normal and abnormal diatheses. As few biological markers have been evaluated as risk factors for psychosis in prodromal patients, the HPA axis and its interaction with intervening life events are apt candidates for study. In this article, we review the HPA axis and its neural effects, present a model for how stress might precipitate psychosis in vulnerable individuals, review the empirical evidence of a link between stress and schizophrenia symptoms, and propose a research design and appropriate statistical models to test the stress-diathesis model for psychosis onset in prodromal patients.

Animals↗
PubMed1983

Historical perspectives in the aetiology of ankylosing spondylitis.

A brief historical review of the aetiology of ankylosing spondylitis is presented. A recurrent theme has been diathesis and infection. Diathesis has now been pinpointed to the 6th chromosome in the form of HLA-B27, but, as yet, we know little of any infective aetiology for ankylosing spondylitis itself.

England↗
PubMed1994

Developmentally moderated expressions of the neuropathology underlying schizophrenia.

A gradually accumulating body of literature suggests that behavioral dysfunction precedes the onset of the schizophrenic syndrome by many years. Thus, a comprehensive neurodevelopmental model of schizophrenia must encompass these early manifestations of dysfunction as well as the postmorbid period. This article draws on previous research findings as well as recently proposed neurodevelopmental models to offer some further hypotheses about the neurodevelopmental process underlying the changing life-course manifestations of the diathesis for schizophrenia. It is proposed that normal maturational events in the central nervous system moderate the behavioral expression of a congenital neuropathology that affects subcortical regions of the brain that are part of multiple neural circuits. Specifically, it is suggested that the diathesis for schizophrenia involves a functional excess of dopamine activity in the basal ganglia that serves to disrupt these circuits. Findings from empirical research suggest a modal developmental trajectory for schizophrenia in which neuromotor dysfunction is most pronounced in early childhood and late in life, whereas florid psychotic symptomatology is most pronounced in late adolescence and early adulthood. The literature on normal central nervous system development suggests that the feedback circuit linking motor cortex with subcortical structures is maximally metabolically activated, relative to other circuits, early and late in the life course. Thus, subcortical dopamine excess may be predominantly expressed in motoric symptoms during these periods. In contrast, late adolescence and early adulthood are marked by low motor cortex metabolic activity relative to other cortical regions, in particular limbic and frontal regions. In addition, hormonal changes appear to result in a maximal activation of the dopamine system during this developmental period. Thus, it is hypothesized that during this period the neural circuitry abnormality will be primarily behaviorally expressed in psychotic symptoms. Some implications of the model for the study of movement abnormalities and psychotic symptoms are discussed.

Adolescent↗